Thursday, 28 April 2016

TOP SCIENTISTS' COLLABORATION ON LYME DISEASE - DIAGNOSTIC TOOLS AND EFFECTIVE CURE




Published on Apr 20, 2016 

Ten of the world's top scientists from leading institutions discuss their scientific insights on the problems and potential solutions for Lyme disease.

Senator Richard Blumenthall US Senate Speech

'The cases of Lyme are exploding in number and their severity impacts our economy as well as quality of life for Americans'

Introduced by David Rothman- Lyme Advocate

CDC reported 10 fold increase in the number of cases in 2013.

Dr Neil Spector Cancer researcher talks about implications in organ donation. He had a heart transplant due to undiagnosed Lyme Disease.


'In the era of genomics are we using archaic unreliable methods to test for Lyme?'

Dr William H Robinson Stanford University talks about the need to develop next generation tests that are much more accurate and sensitive to identify people with Borrelia Burgdorferi as well as other tick borne infections.

Dr Safwan Jaradeh Stanford University Neuromuscular and Neurological faculty. 'Nobody seems to think well could it be something like Lyme.'

Dr Brian Fallon Columbia University 
Director of the Lyme and Tick-borne diseases research center at Columbia.
 says - Lyme can cause many symptoms he talks about a child who manifested with compulsive cycling behaviour and anorexia which was caused by Lyme Disease and with treatment symptoms went away.

Dr Neil Spector goes on to say- 'Over 300000 cases a year I think demands more attention than Zika virus which overnight becomes a W.H.O. global health crisis. So it's not to minimize the problems of Zika but it is saying there are children who are equally suffering with Lyme disease and children who may be through the consequences of Lyme Disease dying and adults dying through consequences of Lyme Disease.

Stand 4 Lyme founder Sherry Cagan and her husband, Laird have joined forces with with Stanford Scientists to pave a medical path to wellness for patients at all stages of Lyme Disease. Stanford collaborative research with Harvard, Johns Hopkins and Columbia Universities. 

Dr Philip A Pizzo Stanford University Professor of Microbiology and Immunology
Dr Pizzo appointed the Stanford Lyme Working group a collaborative effort between Stanford researchers and other major universities.

Dr Laura Roberts Stanford University says 'Lyme Disease has been neglected scientifically with the Lyme disease working group at Stanford and other universities we are hoping to change that.'

Dr William Robinson - 'Lyme disease shares molecular mechanisms with many different diseases both microbial infections as well as certain inflammatory diseases and the work of the Stanford Lyme working group can help uncover these mechanisms.

Irv Weissman MD Stanford University is working on macrophage problems and persistently infected cells.

Dr Nevena Zubcevk Harvard University is working on - ' Testing blood banks for Lyme and co infections' and also clearing up difficulty we are currently having  with 'In utero transmission of Lyme'

John Nathanial Aucott Johns Hopkins University says this has been an ideal collaboration it has really advanced our ability to do research in Lyme Disease, we collaborate with Dr Bill Robinson at Stanford to develop bio markers or tools to better measure Lyme Disease.

Ying Zhang M.D. PhD Johns Hopkins Medicine
 says' Stand 4 Lyme unique strategy in partnership with top notch scientists from Stanford will ensure that best minds and cutting edge research and diagnostic tools are applied to building a more effective cure  for this complex and illusive disease.  

Saturday, 16 April 2016

LYME DISEASE RELIES HEAVILY ON IMPROVING UNDERSTANDING OF THE MECHANISM OF DISEASE TRANSMISSION

Modelling the seasonality of Lyme disease risk and the potential impacts of a warming climate within the heterogeneous landscapes of Scotland

Sen LiLucy GilbertPaula A. HarrisonMark D. A. Rounsevell


Abstract

Lyme disease is the most prevalent vector-borne disease in the temperate Northern Hemisphere. The abundance of infected nymphal ticks is commonly used as a Lyme disease risk indicator. Temperature can influence the dynamics of disease by shaping the activity and development of ticks and, hence, altering the contact pattern and pathogen transmission between ticks and their host animals. A mechanistic, agent-based model was developed to study the temperature-driven seasonality of Ixodes ricinus ticks and transmission of Borrelia burgdorferi sensu lato across mainland Scotland. Based on 12-year averaged temperature surfaces, our model predicted that Lyme disease risk currently peaks in autumn, approximately six weeks after the temperature peak. The risk was predicted to decrease with increasing altitude. Increases in temperature were predicted to prolong the duration of the tick questing season and expand the risk area to higher altitudinal and latitudinal regions. These predicted impacts on tick population ecology may be expected to lead to greater tick–host contacts under climate warming and, hence, greater risks of pathogen transmission. The model is useful in improving understanding of the spatial determinants and system mechanisms of Lyme disease pathogen transmission and its sensitivity to temperature changes.

Friday, 15 April 2016

SHORTCOMINGS OF PLEASE TRIAL LIMITING LYME DISEASE TREATMENT



Published on Apr 13, 2016
Dr. Daniel Cameron discusses the shortcomings of a study published in the New England Journal of Medicine which claims that long-term antibiotics are ineffective in treating persistent Lyme disease symptoms.

Thank you Dr Daniel Cameron for explaining this so well.

I had been interested to hear how this PLEASE trial progressed but very disappointed when I read the published report in the NEJM. 

My interest was specifically because Clarithromycin has been an antibiotic that has helped me recover from my Lyme Disease more than other antibiotics. It was especially helpful when combined with Hydroxychloroquine. (One of the combinations in the trial). However in my case I still very slowly relapse when antibiotics end and quickly improve on further short courses of clarithromycin. 

The only time I have been symptom free was after a recent stay in hospital with Gall bladder problems and a couple of days of IV ceftriaxone followed by a week oral co amoxiclav but once again symptoms slowly returned. 

Without a good Lyme doctor to guide me I wait in hope of results of better research findings than this PLEASE study.

For me for now the best Guidelines are how I respond to treatment.

The NEJM PLEASE study has been much talked about in the press but some of the more interesting comments are those from patients and their doctors who experience Chronic Lyme Disease - the responses to the article are worth a read 




David Michael Connor Huffington Post-


Holly Aherne Poughkeepsie Journal -

Oh! perhaps I should just give a link to the article that has been so poorly received by the Lyme community -  http://www.nejm.org/doi/full/10.1056/NEJMoa1505425#t=article

Wednesday, 30 March 2016

FIRST LYME DISEASE PULSE-DOSING HUMAN TRIALS WITH MEDICAL SCHOOLS

A new regimen
Lewis and his col­leagues are pro­viding that focus. A sub­pop­u­la­tion of B. burgdor­feri cells, they dis­cov­ered ear­lier, are “per­sister” cells—they are alive but lie dor­mant, in a spore­like state. Because antibi­otics attack only actively func­tioning bac­te­rial cells, per­sis­ters escape the onslaught. How­ever, once the antibi­otic has been flushed from the system, the per­sis­ters “wake up,” says Lewis, dividing and mul­ti­plying until an army of progeny infect the host.
That’s where “pulse dosing” comes in. Lewis’ team, in col­lab­o­ra­tion with researchers studying B. burgdor­feri in mice at Tufts University’s Sackler School of Bio­med­ical Sci­ences, has been ana­lyzing the effect of giving the mice an antibi­otic that kills all the actively func­tioning bac­te­rial cells and then—using the timing that erad­i­cated the pathogen in the test tube—giving addi­tional doses to quash the per­sister cells as they begin to wake up but before they reproduce.
Plans are in the works for the first pulse-​​dosing human trials with med­ical schools.

The above extract is from News at Northeastern go to this link to read the full article:-
 http://www.northeastern.edu/news/2016/03/researchers-investigate-four-promising-new-treatments-for-lyme-disease/
 
'Uni­ver­sity Dis­tin­guished Pro­fessor Kim Lewis, who leads the Lyme dis­ease research team, is now expanding that ther­a­peutic reach with the help of a $1.5 mil­lion grant from the Steven and Alexandra Cohen Foundation.

The team is pur­suing four arms of treatment-​​related research at Northeastern’s Antimi­cro­bial Dis­covery Center, which Lewis directs.

They are: a mouse study of a reg­imen that erad­i­cated the bac­terium in the test tube, set­ting the stage for human trials; antibi­otic cock­tails using existing drugs; strate­gies to dis­cover new drugs that selec­tively target the Lyme bac­terium; and ways to alter the com­po­si­tion of the microbiome—the com­mu­nity of microor­gan­isms inhab­iting the human body—to stop the autoim­mune reac­tions that char­ac­terize the disease.
All four show exciting promise. The grant, Lewis says, “will give us the flex­i­bility to test our approaches in par­allel, which will save us an enor­mous amount of time.”

If Lyme is caught early, patients gen­er­ally recover quickly when treated with antibi­otics, pri­marily doxy­cy­line. How­ever, 10 to 20 per­cent of patients go on to develop a debil­i­tating chronic con­di­tion called Post-​​Treatment Lyme Dis­ease Syn­drome, or PTLDS, with symp­toms that include extreme fatigue, arthritis, muscle pain, and cog­ni­tive difficulties.
I find it amazing that when you show up at the doctor’s office you are not told that there is a 10 to 20 per­cent chance that your life as you know it has ended,” says Lewis. “Nobody seems to be focusing on the next step: How to pre­vent the sub­se­quent rise of the chronic condition.”

Earlier posts on Prof Kim Lewis can be found through this link:-
 http://lookingatlyme.blogspot.co.uk/2015/05/borrelia-burgdorferi-lyme-disease-forms.html

Friday, 18 March 2016

NEW STRATEGIES REQUIRED TO CONTROL TICKS AND TICK BORNE DISEASES - CO INFECTION THE RULE

Co-infection of Ticks: The Rule Rather Than the Exception

  • Claire Valiente Moro ,Elise Vaumourin ,Lorraine Michelet ,Florence Hélène Tran ,Elodie Devillers ,
  • Jean-François Cosson ,Patrick Gasqui ,Van Tran Van ,Patrick Mavingui ,Gwenaël Vourc’h ,Muriel Vayssier-Taussat
PLOS
  • Published: March 17, 2016
  • DOI: 10.1371/journal.pntd.0004539

 http://journals.plos.org/plosntds/article?id=10.1371%2Fjournal.pntd.0004539

 

Abstract

Introduction

Ticks are the most common arthropod vectors of both human and animal diseases in Europe, and the Ixodes ricinus tick species is able to transmit a large number of bacteria, viruses and parasites. Ticks may also be co-infected with several pathogens, with a subsequent high likelihood of co-transmission to humans or animals. However few data exist regarding co-infection prevalences, and these studies only focus on certain well-known pathogens. In addition to pathogens, ticks also carry symbionts that may play important roles in tick biology, and could interfere with pathogen maintenance and transmission. In this study we evaluated the prevalence of 38 pathogens and four symbionts and their co-infection levels as well as possible interactions between pathogens, or between pathogens and symbionts.

Methodology/principal findings

A total of 267 Ixodes ricinus female specimens were collected in the French Ardennes and analyzed by high-throughput real-time PCR for the presence of 37 pathogens (bacteria and parasites), by rRT-PCR to detect the presence of Tick-Borne encephalitis virus (TBEV) and by nested PCR to detect four symbionts. Possible multipartite interactions between pathogens, or between pathogens and symbionts were statistically evaluated. Among the infected ticks, 45% were co-infected, and carried up to five different pathogens. When adding symbiont prevalences, all ticks were infected by at least one microorganism, and up to eight microorganisms were identified in the same tick. When considering possible interactions between pathogens, the results suggested a strong association between Borrelia garinii and B. afzelii, whereas there were no significant interactions between symbionts and pathogens.

Conclusion/significance

Our study reveals high pathogen co-infection rates in ticks, raising questions about possible co-transmission of these agents to humans or animals, and their consequences to human and animal health. We also demonstrated high prevalence rates of symbionts co-existing with pathogens, opening new avenues of enquiry regarding their effects on pathogen transmission and vector competence.

Author Summary

Ticks transmit more pathogens than any other arthropod, and one single species can transmit a large variety of bacteria and parasites. Because co-infection might be much more common than previously thought, we evaluated the prevalence of 38 known or neglected tick-borne pathogens in Ixodes ricinus ticks. Our results demonstrated that co-infection occurred in almost half of the infected ticks, and that ticks could be infected with up to five pathogens. Moreover, as it is well established that symbionts can affect pathogen transmission in arthropods, we also evaluated the prevalence of four symbiont species and demonstrated that all ticks were infected by at least one microorganism. This work highlights the co-infection phenomenon in ticks, which may have important implications for human and animal health, emphasizing the need for new diagnostic tests better adapted to tick-borne diseases. Finally, the high co-occurrence of symbionts and pathogens in ticks, reveals the necessity to also account for these interactions in the development of new alternative strategies to control ticks and tick-borne disease.

Wednesday, 16 March 2016

WHAT CAUSES ALZHEIMER'S?

Researchers Identify Virus and Two Types of Bacteria as Major Causes of Alzheimer’s

 'A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.
 http://neurosciencenews.com/microbes-alzheimers-neurology-3826/


Microbes and Alzheimer’s Disease

'AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease [9, 10]. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic'
and 

'In summary, we propose that infectious agents, including HSV1, Chlamydia pneumonia, and spirochetes, reach the CNS and remain there in latent form. These agents can undergo reactivation in the brain during aging, as the immune system declines, and during different types of stress (which similarly reactivate HSV1 in the periphery). The consequent neuronal damage— caused by direct viral action and by virus-induced inflammation— occurs recurrently, leading to (or acting as a cofactor for) progressive synaptic dysfunction, neuronal loss, and ultimately AD. Such damage includes the induction of Aβ which, initially, appears to be only a defense mechanism.'
The above was published March 2016 in ISO Press -
 http://content.iospress.com/articles/journal-of-alzheimers-disease/jad160152



This is a call for research to be done in this important field and to look at antimicrobial therapy as a way forward to treating some cases of Alzheimer's.


'Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said “The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”
The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.'-
http://neurosciencenews.com/microbes-alzheimers-neurology-3826/ 

Many of the media outlets have focused on the aspect of herpes virus and sadly missed the connection with bacteria - notably spirocaetal infections. 
Prof Judith Miklossy was one of the authors of this editorial and her work with Borrelia spirocaetes and dental spirochaetes has been discussed on this blog previously here 
http://lookingatlyme.blogspot.co.uk/search?q=Miklossy

Below is an important presentation from Dr Alan MacDonald on the subject of Borrelia infections of the brain and the development of Alzheimer's Disease.




Review of Infectious Borrelia species Chronic Brain Infections and the Development of Alzheimer's Disease from Alan MacDonald on Vimeo.

Tuesday, 1 March 2016

WHY ARE DOCTORS SO QUICK TO DIAGNOSE AUTOIMMUNE DISEASE? WITHOUT CONSIDERING LYME DISEASE.






Dr. Steven E. Phillips, MD

Lyme Connection / Ridgefield Lyme Disease Task Force